The role increased free radical production associated with mitochondrial dysfunction is well established in the pathophysiology of diabetes mellitus. A male Wistar rat model was utilized in which diabetes was induced by alloxan at a dose of 140mg/kg body weight, intraperitoneally for 8 weeks. In alloxan induced diabetes on the activities of Krebs cycle enzymes, oxidative as well as enzymes involved in oxidative metabolism were altered. Oxidative damage to DNA, protein and lipid were observed, which provide insight into the association of elevated free radicals and mitochondrial dysfunction leading to diabetes mellitus. Lipoic acid treatment (100mg/kg body weight for 30 days orally) restored mitochondrial functioning showing normal activity of TCA cycle enzyme with decreased free radical production and oxidative damage. Thus, our results propose that lipoic acid restores mitochondrial function in experimentally induced diabetic rats through decreasing levels of free radicals and promoting activation of Krebs cycle enzymes.